Ginseng alleviates folliculogenesis disorders via induction of cell proliferation and downregulation of apoptotic markers in nicotine-treated mice.


Journal

Journal of ovarian research
ISSN: 1757-2215
Titre abrégé: J Ovarian Res
Pays: England
ID NLM: 101474849

Informations de publication

Date de publication:
23 Jan 2022
Historique:
received: 14 06 2021
accepted: 05 01 2022
entrez: 24 1 2022
pubmed: 25 1 2022
medline: 17 3 2022
Statut: epublish

Résumé

Ginseng is a powerful phytoestrogen with high antioxidant properties. This study aimed to evaluate the effect of Panax Ginseng (PG) on folliculogenesis, proliferation, and apoptosis in the ovary impaired by nicotine. Forty adult mice were divided into five groups. Control, sham, and nicotine groups, and co-treated groups of nicotine and ginseng in doses of 0.5 and 1 g/kg. Folliculogenesis was assessed via histopathology and serum evaluation of estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) by ELISA. Lipid peroxidation and antioxidant enzyme activities both in homogenate tissue and serum were assayed by colorimetric analysis. Apoptotic markers of cytochrome c (Cyt c), Bax, and Bcl-2 were evaluated by RT-PCR. Proliferative index was studied by the Ki-67 immunostaining procedure. In comparison to the control or sham groups, nicotine significantly reduced the levels of FSH, LH, and estradiol hormones. An insignificant reduction was observed in the progesterone hormone. Nicotine reduced all healthy follicle numbers, except primordial (P = 0.001). Malondialdehyde (MDA) was increased in tissue and serum in the nicotine group (P = 0.01). Serum catalase (CAT) and enzymatic activity of superoxide dismutase (SOD) both were reduced in tissue and the serum, in the nicotine group. Nicotine induced a reduction in the proliferative indexes of granulosa and theca cells in pre-antral and antral follicles (P = 0.001). However, its effect on the proliferative index of stroma cells was not significant. Apoptotic markers were elevated in the nicotine group (P = 0.001). Co-treatment with ginseng elevated all sex hormones, increased healthy follicles, and reduced tissue or serum lipid peroxidation, compared with the nicotine group (p < 0.05). Co-Treatment with ginseng also reduced the expression of apoptotic markers and increased the proliferative indexes in granulosa and theca cells in pre-antral and antral follicles and also in stroma cells, in comparison to the nicotine group (P = 0.001). All above-mentioned alterations following treatment with ginseng were remarkable, especially in the dose of 1 g/kg. This study showed ginseng protects folliculogenesis via alteration of hypothalamic- pituitary-gonadal (HPG) axis, induction of proliferation in ovarian somatic cells, reduction of lipid peroxidation, and downregulation of apoptotic markers in the mouse ovary, treated with nicotine.

Sections du résumé

BACKGROUND BACKGROUND
Ginseng is a powerful phytoestrogen with high antioxidant properties.
OBJECTIVE OBJECTIVE
This study aimed to evaluate the effect of Panax Ginseng (PG) on folliculogenesis, proliferation, and apoptosis in the ovary impaired by nicotine.
METHODS METHODS
Forty adult mice were divided into five groups. Control, sham, and nicotine groups, and co-treated groups of nicotine and ginseng in doses of 0.5 and 1 g/kg. Folliculogenesis was assessed via histopathology and serum evaluation of estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) by ELISA. Lipid peroxidation and antioxidant enzyme activities both in homogenate tissue and serum were assayed by colorimetric analysis. Apoptotic markers of cytochrome c (Cyt c), Bax, and Bcl-2 were evaluated by RT-PCR. Proliferative index was studied by the Ki-67 immunostaining procedure.
RESULTS RESULTS
In comparison to the control or sham groups, nicotine significantly reduced the levels of FSH, LH, and estradiol hormones. An insignificant reduction was observed in the progesterone hormone. Nicotine reduced all healthy follicle numbers, except primordial (P = 0.001). Malondialdehyde (MDA) was increased in tissue and serum in the nicotine group (P = 0.01). Serum catalase (CAT) and enzymatic activity of superoxide dismutase (SOD) both were reduced in tissue and the serum, in the nicotine group. Nicotine induced a reduction in the proliferative indexes of granulosa and theca cells in pre-antral and antral follicles (P = 0.001). However, its effect on the proliferative index of stroma cells was not significant. Apoptotic markers were elevated in the nicotine group (P = 0.001). Co-treatment with ginseng elevated all sex hormones, increased healthy follicles, and reduced tissue or serum lipid peroxidation, compared with the nicotine group (p < 0.05). Co-Treatment with ginseng also reduced the expression of apoptotic markers and increased the proliferative indexes in granulosa and theca cells in pre-antral and antral follicles and also in stroma cells, in comparison to the nicotine group (P = 0.001). All above-mentioned alterations following treatment with ginseng were remarkable, especially in the dose of 1 g/kg.
CONCLUSION CONCLUSIONS
This study showed ginseng protects folliculogenesis via alteration of hypothalamic- pituitary-gonadal (HPG) axis, induction of proliferation in ovarian somatic cells, reduction of lipid peroxidation, and downregulation of apoptotic markers in the mouse ovary, treated with nicotine.

Identifiants

pubmed: 35067219
doi: 10.1186/s13048-022-00945-x
pii: 10.1186/s13048-022-00945-x
pmc: PMC8785492
doi:

Substances chimiques

Apoptosis Regulatory Proteins 0
Hormones 0
Ki-67 Antigen 0
Plant Preparations 0
Malondialdehyde 4Y8F71G49Q
Nicotine 6M3C89ZY6R
Catalase EC 1.11.1.6
Superoxide Dismutase EC 1.15.1.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

14

Subventions

Organisme : guilan university of medical sciences
ID : 96101603
Organisme : guilan university of medical sciences
ID : 2018

Informations de copyright

© 2022. The Author(s).

Références

Biomed Res Int. 2015;2015:767124
pubmed: 25705687
Mol Hum Reprod. 2000 Mar;6(3):232-7
pubmed: 10694270
Int Braz J Urol. 2011 Jul-Aug;37(4):495-506
pubmed: 21888702
Hum Reprod. 1989 Jul;4(5):482-5
pubmed: 2794009
J Ethnopharmacol. 2014 Jul 3;154(3):753-7
pubmed: 24814037
Cell J. 2019 Jul;21(2):210-219
pubmed: 30825295
Biol Reprod. 2005 Mar;72(3):628-32
pubmed: 15548733
Int J Environ Res Public Health. 2009 Feb;6(2):445-62
pubmed: 19440393
Br J Pharmacol. 2017 Jun;174(11):1263-1280
pubmed: 27723080
Exp Gerontol. 2012 Jan;47(1):77-84
pubmed: 22075532
J Ginseng Res. 2015 Jan;39(1):69-75
pubmed: 25535479
Fertil Steril. 1986 Aug;46(2):232-6
pubmed: 3732529
Environ Health Perspect. 2005 Oct;113(10):1285-90
pubmed: 16203235
Sci Rep. 2020 Aug 11;10(1):13551
pubmed: 32782329
J Endocrinol. 1995 Aug;146(2):349-57
pubmed: 7561648
Pflugers Arch. 2013 May;465(5):739-46
pubmed: 23417608
J Ginseng Res. 2011 Jun;35(2):250-5
pubmed: 23717068
JBRA Assist Reprod. 2018 Jun 01;22(2):78-81
pubmed: 29389093
Cell Biol Int. 2010 Jul;34(7):769-75
pubmed: 20402666
Indian J Exp Biol. 1999 Feb;37(2):184-6
pubmed: 10641142
Anal Biochem. 1976 May 7;72:248-54
pubmed: 942051
Endocrine. 2009 Oct;36(2):281-90
pubmed: 19693712
Int J Mol Sci. 2018 Nov 23;19(12):
pubmed: 30477143
J Ginseng Res. 2011 Jun;35(2):129-37
pubmed: 23717054
Toxicol Rep. 2021 Apr 02;8:793-803
pubmed: 33850734
Reprod Toxicol. 2018 Oct;81:132-139
pubmed: 30056207
Endocrinology. 2005 Jun;146(6):2817-26
pubmed: 15731357
Toxicol Appl Pharmacol. 2014 Dec 15;281(3):266-75
pubmed: 25448442
Hum Reprod Update. 2005 Mar-Apr;11(2):162-77
pubmed: 15705959
Soc Reprod Fertil Suppl. 2007;64:141-63
pubmed: 17491145
PLoS One. 2012;7(4):e35538
pubmed: 22514749
Hum Reprod. 2006 Mar;21(3):610-7
pubmed: 16311296
Mol Hum Reprod. 2000 Jan;6(1):19-25
pubmed: 10611256
World J Mens Health. 2015 Dec;33(3):143-60
pubmed: 26770934
Early Pregnancy. 1997 Mar;3(1):34-7
pubmed: 9265557
J Reprod Infertil. 2012 Jul;13(3):143-50
pubmed: 23926539
Cell Mol Biol (Noisy-le-grand). 2018 Oct 30;64(13):97-102
pubmed: 30403603
J Hum Reprod Sci. 2014 Jan;7(1):41-6
pubmed: 24829530
N Engl J Med. 1982 Oct 21;307(17):1062-5
pubmed: 7121516
Neurosci Biobehav Rev. 2016 Jun;65:173-84
pubmed: 27068856
J Clin Endocrinol Metab. 2002 Dec;87(12):5532-8
pubmed: 12466349
Anim Reprod Sci. 2010 Jul;120(1-4):39-46
pubmed: 20378285
Curr Opin Obstet Gynecol. 2016 Aug;28(4):230-5
pubmed: 27285958
Anat Cell Biol. 2021 Jun 30;54(2):232-240
pubmed: 33597315
Acta Histochem. 2020 Feb;122(2):151470
pubmed: 31812447
Hum Reprod Update. 2011 Jan-Feb;17(1):76-95
pubmed: 20685716
Niger J Physiol Sci. 2011 Nov 23;26(1):103-7
pubmed: 22314996
Biopharm Drug Dispos. 2020 Jul;41(7):295-306
pubmed: 32557706
Int J Mol Sci. 2020 Jun 26;21(12):
pubmed: 32604954
J Ovarian Res. 2012 Sep 20;5(1):25
pubmed: 22995067
Drugs R D. 2017 Dec;17(4):615-621
pubmed: 29058303
Arch Med Sci. 2019 Nov 25;16(6):1376-1386
pubmed: 33224337
Reprod Toxicol. 2002 Nov-Dec;16(6):795-800
pubmed: 12401508
Obstet Gynecol Sci. 2021 May;64(3):274-283
pubmed: 33743577
J Ginseng Res. 2017 Apr;41(2):113-119
pubmed: 28413314
J Ginseng Res. 2016 Apr;40(2):185-95
pubmed: 27158240
Theriogenology. 2020 Nov;157:96-109
pubmed: 32810794
Hum Reprod. 2011 Apr;26(4):878-84
pubmed: 21233109
J Ginseng Res. 2020 Nov;44(6):790-798
pubmed: 33192122
Environ Sci Pollut Res Int. 2018 Jul;25(21):21205-21215
pubmed: 29777495
Tob Induc Dis. 2004 Sep 15;2(3):151-61
pubmed: 19570282
Steroids. 2011 Jun;76(7):653-9
pubmed: 21396948
Nat Commun. 2015 Apr 28;6:6934
pubmed: 25917826
Iran J Basic Med Sci. 2018 Jun;21(6):639-644
pubmed: 29942456
Reprod Domest Anim. 2014 Feb;49(1):170-6
pubmed: 24256504
Antioxid Redox Signal. 2020 Dec 8;:
pubmed: 33115254
Interdiscip Toxicol. 2014 Mar;7(1):41-6
pubmed: 26038675
Biol Reprod. 1995 Aug;53(2):295-301
pubmed: 7492681
Antioxid Redox Signal. 2008 Aug;10(8):1375-403
pubmed: 18402550
J Ginseng Res. 2017 Apr;41(2):215-221
pubmed: 28413327
Int J Mol Sci. 2014 May 06;15(5):7827-40
pubmed: 24806341
Reprod Biol. 2020 Mar;20(1):63-74
pubmed: 31918980

Auteurs

Masoumeh Faghani (M)

Department of Anatomy, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.

Sahar Saedi (S)

Department of Anatomy, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.

Korosh Khanaki (K)

Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran.

Fahimeh Mohammadghasemi (F)

Cellular & Molecular Research Center, Department Of Anatomy, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran. parsahistolab@gmail.com.

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Classifications MeSH